Background- A new super-family of non-selective and non-voltage-gated transient receptor potential (TRP) channels, mainly permeable for Ca2+, has recently been described. By using a rat model for permanent occlusion of the left anterior descending (LAD) artery, we have recently shown that TRPV2 is highly expressed on macrophages in the peri-infarct zone 3-5 days post acute myocardial infarction (acute MI). We wished to assess whether the expression levels of TRPV2 are also elevated in circulating monocytes following acute MI in rats as well as in human samples.
Methods- 1. Rats: Whole blood was collected three days after LAD ligation or chest opening only (sham-operated controls). The circulating blood cells were double-stained with anti- rat CD11 b (which recognizes monocytes/macrophages) and anti-rat TRPV2.
- Human: Whole blood samples were collected from patients who underwent coronary angiography and diagnosed with acute MI (ejection fraction < 45) or normal coronaries. The peripheral mononuclear cells (PBMCs) were isolated by ficoll gradient centrifugation and stained with anti-human TRPV2 followed by FITC-conjugated secondary antibody. The percentage of cells positive for TRPV2 was determined by flow cytometry.
Results- TRPV2 expression was similar in circulating monocytes (CD11b-positive cells) of acute MI and sham animals (4.04 ± 0.52% and 4.8± 0.72% in MI versus sham-operated controls, respectively (p=0.5). Similarly, the percentage of monocyes (FCS-A gating for >100 *103) in the ficoll-gradients isolated from human PBMCs was similar between post MI versus patients diagnosed with normal coronaries (5.9± 2.3% and 6.5± 1.9% in post-MI and normal coronaries, respectively; p=0.9).
Conclusion- The data suggest that while TRPV2 expression is augmented in peri-infarct macrophages, TRPV2 expression on circulatory monocytes is similar. We thus assume that overexpression of TRPV2 occurs only upon maturation of monocytes to active macrophages around the infract zone, where this channel may mediate phagocytosis of the dying cardiomyocytes.
